Project 460121
The contribution of CCN proteins to scleroderma fibrosis: cellular and molecular mechanisms
The contribution of CCN proteins to scleroderma fibrosis: cellular and molecular mechanisms
Project Information
| Study Type: | Unclear |
| Research Theme: | Biomedical |
Institution & Funding
| Principal Investigator(s): | Leask, Andrew C |
| Co-Investigator(s): | Aslam, Muhammad N; Postovit, Lynne-Marie; Riser, Bruce L |
| Institution: | University of Saskatchewan |
| CIHR Institute: | Musculoskeletal Health and Arthritis |
| Program: | |
| Peer Review Committee: | Cell Biology - Disease |
| Competition Year: | 2022 |
| Term: | 5 yrs 0 mth |
Abstract Summary
Fibrotic diseases such as scleroderma have limited therapeutic options. These diseases are characterized by extensive scar tissue deposition. The cells (fibroblasts) within the scar are subject to enhanced tension due to the surrounding scar tissue. They also themselves are abnormal in that they exert excessive tension on the scar tissue. It is believed that this excessive tension is responsible for the maintenance of the scar. A protein called CCN2 is expressed specifically in scar tissue and promotes this tension. A related protein CCN3 is not found in scar tissue, but normally acts to inhibit CCN2. We want to test whether CCN3 and peptides derived from CCN3) can block or reverse scleroderma fibrosis. At the end of the funding period, we will design and initiate clinical trials with our peptides to see if we can block fibrosis clinically.
No special research characteristics identified
This project does not include any of the advanced research characteristics tracked in our database.